My friends and colleagues often remark that they hear so much about the epidemic of type 2 diabetes and the emphasis on weight loss, proper diet, and exercise to prevent it, they wonder what’s holding things up? Why can’t diabetes be prevented? What are the barriers?
These are great and relevant questions. What is standing in the way? We know that numerous randomized clinical trials from around the world, each involving thousands of people… from Europe, China, India, and the U.S. … have conclusively shown that lifestyle modification and metformin treatment are successful in the prevention or delay of the onset of type 2 diabetes for at least 10 years. What more need be shown? What more is there for diabetes clinical researchers to do? What’s missing?
We are aware of the American tendency to snack on carbohydrate-rich food throughout the day. So why is it we stubbornly obtain fasting glucose levels in our patients at risk?
It is easy to point the finger at the people who are at risk for type 2 diabetes. After all, isn’t it in their best interest to comply with the recommendations they hear about lifestyle modification? Can’t they watch their diets, exercise more, and take a pill? The answer is that it is not that simple. Carbohydrate-rich foods are the most plentiful and the cheapest to buy and the easiest to grow. These foods along with fat-rich foods can lead to obesity and impaired glucose tolerance. In some parts of the world people do not have access to a broad array of dietary choices because they cannot afford them financially or the food choices simply are not available.
What about exercise and weight loss? That doesn’t cost anything, right? Yes, true enough, exercise has many benefits including weight loss, and it works for many people, but it must be sustained for a lifetime to be effective in the long run. How many of us have the discipline it takes to commit to this? Easy to say, hard to do.
Well, then, how about a pill? Metformin increases sensitivity to the insulin we make ourselves and it is associated with at least mild satiety and weight loss. This drug is successful for many people, but it also is not affordable for many people around the world. In other words, it is comparatively simple to perform the clinical studies to identify preventive measures, but not so simple to implement the lessons we’ve learned to prevent diabetes.
My answer to “what’s missing” is that we have not yet tackled the critical question about implementation. One can explain away the lack of compliance to methods we know will work, but this does not get at the heart of the matter of implementation. We know this to be true from the history of preventing smoking. For years, chronic smokers realized that puffing on a cigarette was not good for them, but it was hard to get them to quit. A compliance problem. Yet, today there has been a dramatic decrease in the number of people who smoke. Why? Drugs were brought into the market place that helped them quit. The Surgeon General of the U.S. pro-actively required stern warning statements on packages of cigarettes. Nothing short of a cultural revolution emerged in which citizens demanded access to restaurants and public buildings where smoking was not allowed because of the risks of secondary smoke inhalation. Does any of this positive experience give us clues to the prevention of type 2 diabetes?
Perhaps it does in some ways. We could certainly encourage the current Surgeon General to be more pro-active in labeling all foods and beverages with warnings about contents that are potentially harmful for people at risk for type 2 diabetes. Conceivably, more intense education about healthy foods could be brought into our primary grade classrooms. There are clearly examples of parents and legislators putting pressure on schools not to have sugar-rich beverages on their campuses. But we are still left with the problem people have who cannot afford or get access to healthier foods in their immediate environs. I think we have a lot more thinking and implementing to do before we can reach the same success with dietary prevention of type 2 diabetes that we have had with smoking cessation.
It strikes me that one thing we have never tried is to have major discussions about implementation. It is not likely that the same clinical researchers who brought us the good news that this disease can be prevented by behavior modification and a drug are going to solve this problem. It seems more likely that social behaviorists, psychologists, legislators, and other professionals who educate and inform the public will do a better job. Perhaps we need to fill the convention centers we frequent with a new breed of thinkers to identify exactly how to overcome the implementation and compliance problems in the diabetes area.
It is easy to point the finger at the people who are at risk for type 2 diabetes. After all, isn’t it in their best interest to comply with the recommendations they hear about lifestyle modification? Can’t they watch their diets, exercise more, and take a pill? The answer is that it is not that simple.
A final thought about another way to think about the problem of the type 2 diabetes epidemic. The medical profession could be more proactive in early treatment as a preventive measure. We have alerted our patients if a fasting glucose level is slightly abnormal with the advice to improve their diet for a year and check their glucose level again next year. Is the strategy of “watchful waiting” good enough? Experience tells us it is not so likely that the fasting glucose level will be any lower in another year. We also know that a fasting glucose level between 100 and 115 mg/dl is associated with a functional defect in beta cells that leads to defective insulin secretion. And we know that a fasting glucose level above 115 mg/dl is almost certainly associated with elevated post-prandial glucose levels.
We are aware of the American tendency to snack on carbohydrate-rich food throughout the day. So why is it we stubbornly obtain fasting glucose levels in our patients at risk? Why don’t we routinely obtain post-prandial measurements as they are the ones most likely to reflect an abnormality that signals future frank diabetes? We know that chronic hyperglycemia has a detrimental effect on existing beta cells. So why do we wait before starting treatment? We do not delay treatment for our patients with elevated prostatic serum antigens or with moderate cardiac arrhythmias.
In other words, perhaps an important thing to do is to prevent progression of mild glucose tolerance to frank diabetes by closely monitoring glucose intolerance and to initiating appropriate therapy much earlier in this disease. Wouldn’t this approach more likely preserve function in abnormal beta cells so they can play their critical role in regulating blood glucose levels?